Highly sensitive acetone sensor based on WO3 nanosheets derived from WS2 nanoparticles with inorganic fullerene-like structures

Metal oxide semiconductor (MOS) gas sensors are promising for applications in environmental monitoring, dangerous gas detection, and disease diagnosis. Seeking for advanced MOS sensing materials that possess high sensitivity and low limit of detection (LOD) at sub-ppm level is a great challenge. Here, we report the first creation of two-dimensional (2D) WO3 nanosheets by annealing of the inorganic fullerene (IF)-like WS2 nanoparticles that were prepared via sulfurization of WO3 nanoparticles. Transformation of WS2 to WO3 was realised during the annealing process, simultaneously accompanied by the collapse of the hollow IF-WS2 structures and the formation of tiny 2D WO3 nanosheets with a lateral size of 40−80 nm. The resulting 2D WO3 nanosheets exhibited highly enhanced acetone-sensing performance in terms of sensitivity, selectivity, and response/recovery rates compared with the WO3 nanoparticles used as precursor for the synthesis of the IF-WS2 nanoparticles. The nanosheets also demonstrated great repeatability, reliable long-term stability, and very low LOD, making them a promising candidate as gas sensor to detect breath acetone

Bacillus subtilis Inhibits Vibrio natriegens-Induced Corrosion via Biomineralization in Seawater

The marine bacterium, Vibrio natriegens, grows quickly in a marine environment and can significantly accelerate the corrosion of steel materials. Here, we present an approach to inhibit V. natriegens-induced corrosion by biomineralization. The corrosion of steel is mitigated in seawater via the formation of a biomineralized film induced by Bacillus subtilis. The film is composed of extracellular polymeric substances (EPS) and calcite, exhibiting stable anti-corrosion activity. The microbial diversity and medium chemistry tests demonstrated that the inhibition of V. natriegens growth by B. subtilis was essential for the formation of the biomineralized film

PM2.5 induced liver lipid metabolic disorders in C57BL/6J mice

PM2.5 can cause adverse health effects via several pathways, such as inducing pulmonary and systemic inflammation, penetration into circulation, and activation of the autonomic nervous system. In particular, the impact of PM2.5 exposure on the liver, which plays an important role in metabolism and detoxification to maintain internal environment homeostasis, is getting more attention in recent years. In the present study, C57BL/6J mice were randomly assigned and treated with PM2.5 suspension and PBS solution for 8 weeks. Then, hepatic tissue was prepared and identified by metabolomics analysis and transcriptomics analysis. PM2.5 exposure can cause extensive metabolic disturbances, particularly in lipid and amino acids metabolic dysregulation.128 differential expression metabolites (DEMs) and 502 differently expressed genes (DEGs) between the PM2.5 exposure group and control group were detected. The Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that DEGs were significantly enriched in two disease pathways, non-alcoholic fatty liver disease (NAFLD) and type II diabetes mellitus (T2DM), and three signaling pathways, which are TGF-beta signaling, AMPK signaling, and mTOR signaling. Besides, further detection of acylcarnitine levels revealed accumulation in liver tissue, which caused restricted lipid consumption. Furthermore, lipid droplet accumulation in the liver was confirmed by Oil Red O staining, suggesting hepatic steatosis. Moreover, the aberrant expression of three key transcription factors revealed the potential regulatory effects in lipid metabolic disorders, the peroxisomal proliferative agent-activated receptors (PPARs) including PPARα and PPARγ is inhibited, and the activated sterol regulator-binding protein 1 (SREBP1) is overexpressed. Our results provide a novel molecular and genetic basis for a better understanding of the mechanisms of PM2.5 exposure-induced hepatic metabolic diseases, especially in lipid metabolism

Microscopical observation of the marine bacterium vibrio natriegeus growth on metallic corrosion

Biofilm formation and the adsorption of nonsulfate-reducing marine bacterium Vibrio natriegens (V. natriegens) to different metallic surfaces have been studied by atomic force microscopy (AFM). The nature of extracellular polymeric substance (EPS) has been monitored through the force-distance curve. EPS may act as adhesive binding adjacent cells and thus further enhance the aggregation of microbes during cluster formation due to its adhesiveness in nature. The AFM images supplied the change of the morphology of microbial cells and colonies, the distribution of microbial colonies, and the presence of EPS on the surfaces with immersion. Results showed that the biofilms formed on the surfaces increased in thickness and heterogeneity with time and that 3–7 days was the proliferation period of the bacteria on metallic surfaces. The corrosion type of the metals by V. natriegens could be confirmed as typical pitting attack through scanning electron microscopy (SEM) observation

Promoting Barrier Performance and Cathodic Protection of Zinc-Rich Epoxy Primer via Single-Layer Graphene

The effect of single-layer graphene sheets (Gr) on the corrosion protection of zinc-rich epoxy primers (ZRPs) was investigated. Scanning electron microscopy (SEM) with an energy dispersive spectrometer (EDS) were used to characterize morphology and composition of the coatings after immersion for 25 days. The cross-sectional SEM images and X-ray photoelectron spectroscopy (XPS) confirmed that the addition of single-layer graphene facilitated assembling of zinc oxides on the interface between the coating and the steel. The open circuit potential (OCP), electrochemical impedance spectroscopy (EIS) measurements revealed that both the cathodic protection and barrier performance of the ZRP were enhanced after addition of 0.6 wt. % Gr (Gr0.6-ZRP). In addition, the cathodic protection property of the Gr0.6-ZRP was characterized quantitatively by localized electrochemical impedance spectroscopy (LEIS) in the presence of an artificial scratch on the coating. The results demonstrate that moderate amounts of single-layer graphene can significantly improve corrosion resistance of ZRP, due to the barrier protection and cathodic protection effects

IDH2/R140Q mutation confers cytokine-independent proliferation of TF-1 cells by activating constitutive STAT3/5 phosphorylation

Abstract Background R140Q mutation in isocitrate dehydrogenase 2 (IDH2) promotes leukemogenesis. Targeting IDH2/R140Q yields encouraging therapeutic effects in the clinical setting. However, therapeutic resistance occurs in 12% of IDH2/R140Q inhibitor treated patients. The IDH2/R140Q mutant converted TF-1 cells to proliferate in a cytokine-independent manner. This study investigated the signaling pathways involved in TF-1(R140Q) cell proliferation conversion as alternative therapeutic strategies to improve outcomes in patients with acute myeloid leukemia (AML) harboring IDH2/R140Q. Methods The effects of IDH2/R140Q mutation on TF-1 cell survival induced by GM-CSF withdrawal were evaluated using flow cytometry assay. The expression levels of apoptosis-related proteins, total or phosphorylated STAT3/5, ERK, and AKT in wild-type TF-1(WT) or TF-1(R140Q) cells under different conditions were evaluated using western blot analysis. Cell viability was tested using MTT assay. The mRNA expression levels of GM-CSF, IL-3, IL-6, G-CSF, leukemia inhibitory factor (LIF), oncostatin M (OSM), and IL-11 in TF-1(WT) and TF-1(R140Q) cells were quantified via RT-PCR. The secretion levels of GM-CSF, OSM, and LIF were determined using ELISA. Results Our results showed that STAT3 and STAT5 exhibited aberrant constitutive phosphorylation in TF-1(R140Q) cells compared with TF-1(WT) cells. Inhibition of STAT3/5 phosphorylation suppressed the cytokine-independent proliferation of TF-1(R140Q) cells. Moreover, the autocrine GM-CSF, LIF and OSM levels increased, which is consistent with constitutive STAT5/3 activation in TF-1(R140Q) cells, as compared with TF-1(WT) cells. Conclusions The autocrine cytokines, including GM-CSF, LIF, and OSM, contribute to constitutive STAT3/5 activation in TF-1(R140Q) cells, thereby modulating IDH2/R140Q-mediated malignant proliferation in TF-1 cells. Targeting STAT3/5 phosphorylation may be a novel strategy for the treatment of AML in patients harboring the IDH2/R140Q mutation. Video Abstrac

LCAT, ApoD, and ApoA1 Expression and Review of Cholesterol Deposition in the Cornea

Lecithin:cholesterol acyltransferase (LCAT) is an enzyme secreted by the liver and circulates with high-density lipoprotein (HDL) in the blood. The enzyme esterifies plasma cholesterol and increases the capacity of HDL to carry and potentially remove cholesterol from tissues. Cholesterol accumulates within the extracellular connective tissue matrix of the cornea stroma in individuals with genetic deficiency of LCAT. LCAT can be activated by apolipoproteins (Apo) including ApoD and ApoA1. ApoA1 also mediates cellular synthesis of HDL. This study examined the expression of LCAT by epithelial cells, keratocytes, and endothelial cells, the cell types that comprise from anterior to posterior the three layers of the cornea. LCAT and ApoD were immunolocalized to all three cell types within the cornea, while ApoA1 was immunolocalized to keratocytes and endothelium but not epithelium. In situ hybridization was used to detect LCAT, ApoD, and ApoA1 mRNA to learn what cell types within the cornea synthesize these proteins. No corneal cells showed mRNA for ApoA1. Keratocytes and endothelium both showed ApoD mRNA, but epithelium did not. Epithelium and endothelium both showed LCAT mRNA, but despite the presence of LCAT protein in keratocytes, keratocytes did not show LCAT mRNA. RNA sequencing analysis of serum-cultured dedifferentiated keratocytes (commonly referred to as corneal stromal fibroblasts) revealed the presence of both LCAT and ApoD (but not ApoA1) mRNA, which was accompanied by their respective proteins detected by immunolabeling of the cultured keratocytes and Western blot analysis of keratocyte lysates. The results indicate that keratocytes in vivo show both ApoA1 and LCAT proteins, but do not synthesize these proteins. Rather, keratocytes in vivo must take up ApoA1 and LCAT from the corneal interstitial tissue fluid

Highly Stable Aqueous Zinc Metal Batteries Enabled by an Ultrathin Crack‐Free Hydrophobic Layer with Rigid Sub‐Nanochannels

Abstract Aqueous zinc‐metal batteries (AZMBs) have received tremendous attentions due to their high safety, low cost, environmental friendliness, and simple process. However, zinc‐metal still suffer from uncontrollable dendrite growth and surface parasitic reactions that reduce the Coulombic efficiency (CE) and lifetime of AZMBs. These problems which are closely related to the active water are not well‐solved. Here, an ultrathin crack‐free metal–organic framework (ZIF‐7x‐8) with rigid sub‐nanopore (0.3 nm) is constructed on Zn‐metal to promote the de‐solvation of zinc‐ions before approaching Zn‐metal surface, reduce the contacting opportunity between water and Zn, and consequently eliminate water‐induced corrosion and side‐reactions. Due to the presence of rigid and ordered sub‐nanochannels, Zn‐ions deposits on Zn‐metal follow a highly ordered manner, resulting in a dendrite‐free Zn‐metal with negligible by‐products, which significantly improve the reversibility and lifespan of Zn‐metals. As a result, Zn‐metal protected by ultrathin crack‐free ZIF‐7x‐8 layer exhibits excellent cycling stability (over 2200 h) and extremely‐high 99.96% CE during 6000 cycles. The aqueous PANI‐V2O5//ZIF‐7x‐8@Zn full‐cell preserves 86% high‐capacity retention even after ultra‐long 2000 cycles. The practical pouch‐cell can also be cycled for more than 120 cycles. It is believed that the simple strategy demonstrated in this work can accelerate the practical utilizations of AZMBs